Abstract
The first published case of Diabetic Ketoacidosis-induced Takotsubo cardiomyopathy was in 2009. Our patient is the 1st reported case of Diabetic Ketoacidosis- (DKA-) induced Takotsubo cardiomyopathy (TC) in a patient with known hypertrophic cardiomyopathy (HOCM) in the United States. In the literature, there are only two examples linking DKA to TC; however, this report focuses on the biochemical and physiological causes of TC in a patient with known HOCM and new-onset DKA. TC in previously diagnosed HOCM poses particular complications. With the above patient's baseline outflow tract obstruction due to septal hypertrophy, the acute reduction in EF due to TC resulted in transient drop in brain perfusion and, therefore, syncope.
Highlights
The most common documented cause of Takotsubo cardiomyopathy (TC) is a neurohormonal release of catecholamines. In this case report of a man presenting with syncope, we describe Diabetic Ketoacidosis (DKA) as the physiological stressor leading to TC
When DKA was treated and glucose levels were brought within normal range, repeat echo revealed an improved ejection fraction (EF) and normal ventricular motion and, overall resolution of TC
The excess stress-induced catecholamines have the greatest effect on the cardiac apex due to its high
Summary
The most common documented cause of Takotsubo cardiomyopathy (TC) is a neurohormonal release of catecholamines In this case report of a man presenting with syncope, we describe DKA as the physiological stressor leading to TC. Upon workup for this patient’s loss of consciousness, initial labs revealed a metabolic acidotic state and a glucose level of 526 mg/dL. When DKA was treated and glucose levels were brought within normal range, repeat echo revealed an improved EF and normal ventricular motion and, overall resolution of TC. The patient is a 66-year-old male with a history of hypertension, hypertrophic obstructive cardiomyopathy, Meniere’s disease with intermittent lightheadedness, and gait instability that is controlled with intermittent prednisone His usual symptoms progressively worsened with new polyuria, polydipsia, decreased oral intake, and nausea. EKG showed atrial fibrillation with rapid ventricular response as well as ST elevations in leads II, III, aVF, and V3–V6 (Figure 1)
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